CIGARETTE-SMOKING RENDERS LDL SUSCEPTIBLE TO PEROXIDATIVE MODIFICATION AND ENHANCED METABOLISM BY MACROPHAGES
CIGARETTE-SMOKING RENDERS LDL SUSCEPTIBLE TO PEROXIDATIVE MODIFICATION AND ENHANCED METABOLISM BY MACROPHAGES
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DOI：
10.1016/0021-9150(89)90130-5
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发表时间：
1989-10-01
期刊：
影响因子：
5.3
通讯作者：
STEIN, Y
中科院分区：
文献类型：
--
作者：
HARATS, D;BENNAIM, M;STEIN, Y
本文研究了16名23-56岁吸烟者和12名年龄相仿的非吸烟者血浆低密度脂蛋白（LDL）过氧化反应的影响。要求吸烟者在测试前24-40小时不要吸烟。通过测定新鲜血浆和LDL中的硫代巴比妥酸反应物质（TBARS）以及腹腔巨噬细胞对125 I-LDL代谢的增加来评估过氧化作用。吸烟者和不吸烟者新鲜制备的血浆或LDL中的TBARS没有差异。然而，低密度脂蛋白的吸烟者，条件与牛主动脉平滑肌细胞（SMC）孵育，有2倍或更高的TBARS值相比，SMC条件的低密度脂蛋白的非吸烟者。2-4-当比较在吸6-7支香烟（时间0）之前从血浆中分离的LDL和在吸6-7支香烟之后90分钟从血浆中分离的同一个体的LDL时，在SMC调节的LDL中也观察到高1倍的TBARS值。SMC条件125 I-LDL的代谢由腹腔巨噬细胞进行了检查; LDL从血浆中分离的吸烟者在0时被代谢的两倍，积极的LDL的非吸烟者和进一步增加，看到与LDL分离后90分钟急性吸烟。目前的研究结果表明，吸烟使血浆LDL更容易受到随后的过氧化修饰的细胞元素。
The effect of cigarette smoking on peroxidation of plasma low density lipoprotein (LDL) was studied in 16 smokers aged 23-56 years; 12 nonsmokers of similar age served as controls. The smokers were asked to refrain from smoking 24-40 h prior to testing. Peroxidation was assessed by determination of thiobarbituric acid reactive substances (TBARS) in fresh plasma and LDL and by an increase in 125I-LDL metabolism by peritoneal macrophages. There was no difference in TBARS in freshly prepared plasma or LDL of smokers and nonsmokers. However, LDL of smokers, conditioned by incubation with bovine aortic smooth muscle cells (SMC), had 2-fold or higher TBARS values when compared to SMC conditioned LDL of nonsmokers. 2-4-fold higher TBARS values were seen also in SMC conditioned LDL when the comparison was made between LDL isolated from plasma before smoking of 6-7 cigarettes (time 0), and LDL of the same individual isolated from plasma 90 min thereafter. The metabolism of SMC conditioned 125I-LDL by peritoneal macrophages was examined; LDL isolated from plasma of smokers at time 0 was metabolized twice as avidly as LDL of nonsmokers and a further increase was seen with LDL isolated 90 min after acute smoking. The present results indicate that cigarette smoking renders plasma LDL more susceptible to subsequent peroxidative modification by cellular elements.